44
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      ENDOTHELIAL PROGENITOR CELL NUMBER AND COLONY-FORMING CAPACITY IN OVERWEIGHT AND OBESE ADULTS

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective

          To investigate whether adiposity influences endothelial progenitor cell (EPC) number and colony-forming capacity.

          Design

          Cross-sectional study of normal weight, overweight and obese adult humans.

          Subjects

          Sixty-seven sedentary adults (age 45–65y): 25 normal weight (BMI ≤ 25 kg/m 2; 12 males/13 females); 18 overweight (BMI = 25–29.9 kg/m 2; 12 males/6 females); and 24 obese (BMI ≥ 30 kg/m 2; 18 males/6 females). All subjects were non-smokers and free of overt cardiometabolic disease.

          Measurements

          Peripheral blood samples were collected and circulating EPC number was assessed by flow cytometry. Putative EPCs were defined as CD45 /CD34 +/VEGFR-2 +/CD133 + or CD45 /CD34 + cells. EPC colony-forming capacity was measured in vitro using a colony-forming unit assay.

          Results

          Number of circulating putative EPCs (either CD45 /CD34 +/VEGFR-2 +/CD133 + or CD45 /CD34 + cells) was lower (P<0.05) in obese (0.0007±0.0001%; 0.050±0.006%) compared with overweight (0.0016±0.0004%; 0.089±0.019%) and normal weight (0.0015±0.0003%; 0.082±0.008%) adults. There were no differences in EPC number between the overweight and normal weight groups. EPC colony-formation was significantly less in the obese (6±1) and overweight (4±1) compared with normal weight (9±2) adults.

          Conclusion

          These results indicate that: 1) the number of circulating EPCs is lower in obese compared with overweight and normal weight adults; and 2) EPC colony-forming capacity is blunted in overweight and obese adults compared with normal weight adults. Impairments in EPC number and function may contribute to adiposity-related cardiovascular risk.

          Related collections

          Most cited references52

          • Record: found
          • Abstract: found
          • Article: not found

          Number and migratory activity of circulating endothelial progenitor cells inversely correlate with risk factors for coronary artery disease.

          Recent studies provide increasing evidence that postnatal neovascularization involves bone marrow-derived circulating endothelial progenitor cells (EPCs). The regulation of EPCs in patients with coronary artery disease (CAD) is unclear at present. Therefore, we determined the number and functional activity of EPCs in 45 patients with CAD and 15 healthy volunteers. The numbers of isolated EPCs and circulating CD34/kinase insert domain receptor (KDR)-positive precursor cells were significantly reduced in patients with CAD by approximately 40% and 48%, respectively. To determine the influence of atherosclerotic risk factors, a risk factor score including age, sex, hypertension, diabetes, smoking, positive family history of CAD, and LDL cholesterol levels was used. The number of risk factors was significantly correlated with a reduction of EPC levels (R=-0.394, P=0.002) and CD34-/KDR-positive cells (R=-0.537, P<0.001). Analysis of the individual risk factors demonstrated that smokers had significantly reduced levels of EPCs (P<0.001) and CD34-/KDR-positive cells (P=0.003). Moreover, a positive family history of CAD was associated with reduced CD34-/KDR-positive cells (P=0.011). Most importantly, EPCs isolated from patients with CAD also revealed an impaired migratory response, which was inversely correlated with the number of risk factors (R=-0.484, P=0.002). By multivariate analysis, hypertension was identified as a major independent predictor for impaired EPC migration (P=0.043). The present study demonstrates that patients with CAD revealed reduced levels and functional impairment of EPCs, which correlated with risk factors for CAD. Given the important role of EPCs for neovascularization of ischemic tissue, the decrease of EPC numbers and activity may contribute to impaired vascularization in patients with CAD. The full text of this article is available at http://www.circresaha.org.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Endothelial progenitor cells: characterization and role in vascular biology.

            Infusion of different hematopoietic stem cell populations and ex vivo expanded endothelial progenitor cells augments neovascularization of tissue after ischemia and contributes to reendothelialization after endothelial injury, thereby, providing a novel therapeutic option. However, controversy exists with respect to the identification and the origin of endothelial progenitor cells. Overall, there is consensus that endothelial progenitor cells can derive from the bone marrow and that CD133/VEGFR2 cells represent a population with endothelial progenitor capacity. However, increasing evidence suggests that there are additional bone marrow-derived cell populations (eg, myeloid cells, "side population" cells, and mesenchymal cells) and non-bone marrow-derived cells, which also can give rise to endothelial cells. The characterization of the different progenitor cell populations and their functional properties are discussed. Mobilization and endothelial progenitor cell-mediated neovascularization is critically regulated. Stimulatory (eg, statins and exercise) or inhibitory factors (risk factors for coronary artery disease) modulate progenitor cell levels and, thereby, affect the vascular repair capacity. Moreover, recruitment and incorporation of endothelial progenitor cells requires a coordinated sequence of multistep adhesive and signaling events including adhesion and migration (eg, by integrins), chemoattraction (eg, by SDF-1/CXCR4), and finally the differentiation to endothelial cells. This review summarizes the mechanisms regulating endothelial progenitor cell-mediated neovascularization and reendothelialization.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Ischemia- and cytokine-induced mobilization of bone marrow-derived endothelial progenitor cells for neovascularization.

              Endothelial progenitor cells (EPCs) have been isolated from circulating mononuclear cells in human peripheral blood and shown to be incorporated into foci of neovascularization, consistent with postnatal vasculogenesis. We determined whether endogenous stimuli (tissue ischemia) and exogenous cytokine therapy (granulocyte macrophage-colony stimulating factor, GM-CSF) mobilize EPCs and thereby contribute to neovascularization of ischemic tissues. The development of regional ischemia in both mice and rabbits increased the frequency of circulating EPCs. In mice, the effect of ischemia-induced EPC mobilization was demonstrated by enhanced ocular neovascularization after cornea micropocket surgery in mice with hindlimb ischemia compared with that in non-ischemic control mice. In rabbits with hindlimb ischemia, circulating EPCs were further augmented after pretreatment with GM-CSF, with a corresponding improvement in hindlimb neovascularization. There was direct evidence that EPCs that contributed to enhanced corneal neovascularization were specifically mobilized from the bone marrow in response to ischemia and GM-CSF in mice transplanted with bone marrow from transgenic donors expressing beta-galactosidase transcriptionally regulated by the endothelial cell-specific Tie-2 promoter. These findings indicate that circulating EPCs are mobilized endogenously in response to tissue ischemia or exogenously by cytokine therapy and thereby augment neovascularization of ischemic tissues.
                Bookmark

                Author and article information

                Journal
                101256108
                32579
                Int J Obes (Lond)
                International journal of obesity (2005)
                0307-0565
                1476-5497
                28 November 2008
                16 December 2008
                February 2009
                1 August 2009
                : 33
                : 2
                : 219-225
                Affiliations
                [1 ] Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado 80309
                [2 ] Department of Medicine, University of Colorado at Denver and Health Sciences Center, Denver, Colorado 80262
                [3 ] Denver Health Medical Center, Denver, Colorado 80204
                Author notes
                Corresponding author: Christopher DeSouza, Ph.D., Integrative Vascular Biology Laboratory, Department of Integrative Physiology, 354 UCB, University of Colorado, Boulder, CO 80309, Ph: 303 492 2988, Fax: 303 492 6778, E-mail: desouzac@ 123456colorado.edu
                Article
                nihpa79433
                10.1038/ijo.2008.262
                2643316
                19079361
                c1d5cdd0-0f0f-4448-8348-68201eb6ebd3
                History
                Funding
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Award ID: R01 HL077450-04 ||HL
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Award ID: R01 HL076434-05 ||HL
                Categories
                Article

                Nutrition & Dietetics
                obesity,colony-forming units,overweight,endothelial progenitor cells
                Nutrition & Dietetics
                obesity, colony-forming units, overweight, endothelial progenitor cells

                Comments

                Comment on this article